| Autor: |
Brandt MJV; Department for Developmental Origins of Disease, University Medical Center Utrecht Brain Center and Wilhelmina Children's Hospital, Utrecht University, 3508 AB Utrecht, The Netherlands., Nijboer CH; Department for Developmental Origins of Disease, University Medical Center Utrecht Brain Center and Wilhelmina Children's Hospital, Utrecht University, 3508 AB Utrecht, The Netherlands., Nessel I; Centre for Neuroscience, Surgery and Trauma, Blizard Institute, Queen Mary University of London, London E1 2AD, UK., Mutshiya TR; Centre for Neuroscience, Surgery and Trauma, Blizard Institute, Queen Mary University of London, London E1 2AD, UK., Michael-Titus AT; Centre for Neuroscience, Surgery and Trauma, Blizard Institute, Queen Mary University of London, London E1 2AD, UK., Counotte DS; Danone Nutricia Research, 3508 TC Utrecht, The Netherlands., Schipper L; Danone Nutricia Research, 3508 TC Utrecht, The Netherlands., van der Aa NE; Department of Neonatology, University Medical Center Utrecht Brain Center and Wilhelmina Children's Hospital, Utrecht University, 3508 AB Utrecht, The Netherlands., Benders MJNL; Department of Neonatology, University Medical Center Utrecht Brain Center and Wilhelmina Children's Hospital, Utrecht University, 3508 AB Utrecht, The Netherlands., de Theije CGM; Department for Developmental Origins of Disease, University Medical Center Utrecht Brain Center and Wilhelmina Children's Hospital, Utrecht University, 3508 AB Utrecht, The Netherlands. |
| Abstrakt: |
Perinatal hypoxia-ischemia (HI) is a major cause of neonatal brain injury, leading to long-term neurological impairments. Medical nutrition can be rapidly implemented in the clinic, making it a viable intervention to improve neurodevelopment after injury. The omega-3 ( n -3) fatty acids docosahexaenoic acid (DHA, 22:6 n -3) and eicosapentaenoic acid (EPA, 20:5 n -3), uridine monophosphate (UMP) and choline have previously been shown in rodents to synergistically enhance brain phospholipids, synaptic components and cognitive performance. The objective of this study was to test the efficacy of an experimental diet containing DHA, EPA, UMP, choline, iodide, zinc, and vitamin B12 in a mouse model of perinatal HI. Male and female C57Bl/6 mice received the experimental diet or an isocaloric control diet from birth. Hypoxic ischemic encephalopathy was induced on postnatal day 9 by ligation of the right common carotid artery and systemic hypoxia. To assess the effects of the experimental diet on long-term motor and cognitive outcome, mice were subjected to a behavioral test battery. Lesion size, neuroinflammation, brain fatty acids and phospholipids were analyzed at 15 weeks after HI. The experimental diet reduced lesion size and neuroinflammation specifically in males. In both sexes, brain n -3 fatty acids were increased after receiving the experimental diet. The experimental diet also improved novel object recognition, but no significant effects on motor performance were observed. Current data indicates that early life nutritional supplementation with a combination of DHA, EPA, UMP, choline, iodide, zinc, and vitamin B12 may provide neuroprotection after perinatal HI. |
